Extravascular foci ofTrypanosoma vivaxin goats: the central nervous system and aqueous humor of the eye as potential sources of relapse infections after chemotherapy

Abstract

Relapse of parasitaemia after drug treatment of trypanosome infection is normally attributed to drug-resistance on the part of the parasite, under-dosage of the drug or reinfection of the host. In addition, inaccessibility of parasites to drug through sequestration in privileged extravascular sites has been shown in the past to occur with Trypanosoma brucei, and we have obtained evidence that extravascular foci of T. vivax can also serve as a source of relapsing infections. Infection of goats with a West African stock of T. vivax resulted in severe illness, which was fatal if untreated. During the terminal stage of an acute infection, clinical signs of central nervous system involvement were apparent. Histologically, the choroid plexus was swollen and oedematous, and in some cases meningitis or meningoencephalitis was seen. Trypanosomes could be detected in the cerebrospinal fluid, and also extravascularly in the choroid plexus and meninges. In three cases they were present in the aqueous humor, associated with corneal cloudiness or opacity. Treatment of 2 goats with the trypanocidal drug diminazene aceturate eliminated parasitaemia, but infections in both relapsed about 6 weeks later, despite trypanosomes being undetectable in the bloodstream during the intervening period. We conclude that the relapse infections were caused by reemergence of trypanosomes from the CNS and/or the eye, where sequestered parasites may have been inaccessible to the trypanocide.

Evaluation of clinical signs, parasitemia, hematologic and biochemical changes in cattle experimentally infected with Trypanosoma vivax

“…Paiva et al (2000) believe that adaptation to the mechanical transmission has decreased antigenic variation of VSG, however Dagnachew et al (2015) observed that T. vivax strains from areas without tsetse (only mechanical transmission occurs) are as pathogenic as those from areas with cyclical transmission. Another explanation for the persistence of the infection is refuge points with subsequent lapses in infection such as cerebrospinal fluid and aqueous humor (WHITELAW et al, 1988). The presence of T. vivax in the cerebrospinal fluid was observed and correlated with central nervous system damage in chronically infected goats.…”

Trypanosoma (Duttonella) vivax: its biology, epidemiology, pathogenesis, and introduction in the New World - a review

“…Animals recovering from the disease can become reservoirs, with low or even undetectable blood levels of the parasite (Plata 1931b). In the aparasitemic phases, trypanosomes can be found extravascularly, in lymph nodes (Hoare 1972), eyes (in the choroid plexus and aqueous humor) (Whitelaw et al 1988), and cerebrospinal fluid (Tuntasuvan et al 1997). Occult infections can be reactivated by stress.…”

Trypanosoma vivax nos tecidos testicular e epididimário de ovinos experimentalmente infectados

“…Tal fato tem grande importância na fisiopatogenia das lesões inflamatórias e degenerativas descritas no coração (Masake 1980) e sistema nervoso (Whitelaw et al 1988) de caprinos infectados experimentalmente por T. vivax.…”

“…vivax já foi identificado no sistema nervoso central, humor vítreo (Whitelaw et al 1988) e miocárdio (Kimeto et al 1990) onde foi apontado como causador de patologias nessas regiões. Entretanto, ainda não se encontrou relatos da presença do parasita no parênquima de órgãos reprodutivos.…”